[New aspects of the blood flow-augmenting and insulin-like activity of muscle exercise: possible involvement of the kallikrein-kinin-prostaglandin system (author's transl)].
Adaptations of energy metabolism, as they occur during contractions of skeletal muscle besides by anaerobic glycolysis are achieved via changes in capillary blood flow providing substrates and oxygen for combustion. Since, initially, oxygen supply is restricted in the working muscle, glucose would seem to be the adequate fuel as it may be used anaerobically and yields more energy per mole of oxygen than fatty acids under such circumstances. Besides glucose, amino acids are also required for accelerated proteosynthesis according to the work load. Therefore, an enlargement of the capillary net has to be accompanied by an amplification of the action of insulin, which is often present in only small amounts, e.g., after an overnight fast. This aim is met in three ways: (1) enlargement of the capillary net with accelerated blood flow increasing the supply of insulin and the number of receptor sites for insulin binding; (2) accelerated transport of insulin through the capillary wall, providing more insulin in the interstitial space and at the plasma membranes; (3) a molecular mechanism directly involving the insulin-receptor-messenger complex, localized at the plasma membrane of the working muscle cell. These mechanisms resemble a self-regulatory process, set in motion by the release of metabolites from the working tissue. From recent studies there is accumulating evidence that kinins liberated from their precursors are involved as tissue hormones by carrying the signal across the interstitial space to the smooth muscle cells of the capillary vessels. Concomitantly, prostaglandins are released intracellularly to bring about, in cooperation with kinins, the various adaptive mechanisms. Amplifying systems of this kind may play a role not only in muscle but also in other tissues where adequate kinin or prostaglandin release would appear beneficial under several clinical conditions such as shock, coronary infarction, wound healing, etc.
D001920:Bradykinin / Q000008:administration & dosage; D002196:Capillaries / Q000502:physiology*; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000502:physiology; D007610:Kallikreins / Q000502:physiology*; D007705:Kinins / Q000502:physiology*; D009119:Muscle Contraction; D009132:Muscles / Q000098:blood supply; D009584:Nitrogen / Q000378:metabolism; D010101:Oxygen Consumption; D010288:Parenteral Nutrition; D011453:Prostaglandins / Q000502:physiology*; D011480:Protease Inhibitors / Q000502:physiology; D011972:Receptor, Insulin / Q000502:physiology
D007328:Insulin; D007705:Kinins; D011453:Prostaglandins; D011480:Protease Inhibitors; D011972:Receptor, Insulin; D007610:Kallikreins; D005947:Glucose; D009584:Nitrogen; D001920:Bradykinin
Neue Aspekte zur durchblutungssteigernden und insulinähnlichen Wirkung der Muskelarbeit: Mögliche Beteiligung des Kallikrein-Kinin-Prostaglandin Systems.